| 摘要: |
| 目的:探讨积雪草酸调控白细胞介素(IL)-6/ 信号转导子和转录激活子3(STAT3) / 核转录因子-κB(NF-κB)通路对哮喘
小鼠Treg/ Th17 免疫平衡的影响。方法:采用卵清蛋白(OVA)致敏和激发来制备哮喘小鼠模型,随机分为模型组、积雪草酸低
剂量组(54 mg/ kg)、积雪草酸高剂量组(108 mg/ kg)、积雪草酸高剂量(108 mg/ kg)+Colivelin(IL-6/ STAT3/ NF-κB 激活剂,2 mg/ kg)组,
每组各10 只。另选10 只小鼠在致敏和激发阶段给予等剂量生理盐水设为对照组,用积雪草酸和Colivelin 分组处理各组小鼠
后检测其肺组织病理形态,肺泡灌洗液(BALF)中炎性细胞计数,外周血Treg/ Th17,BALF 和血清中Treg、Th17 细胞分泌因子水
平,肺组织IL-6/ STAT3/ NF-κB 通路相关蛋白表达。结果:与对照组比较,模型组小鼠肺组织发生明显病理损伤,外周血Treg 细
胞占比和Treg/ Th17,BALF 和血清IL-10、IL-35 水平降低(P<0. 05)。肺部炎症评分,BALF 中白细胞计数与嗜酸粒细胞计数,外
周血Th17 细胞占比,BALF 和血清IL-17、IL-6 水平,肺组织IL-6 蛋白表达与p-STAT3/ STAT3、p-NF-κB p65/ NF-κB p65 升高(P<
0. 05)。低、高剂量积雪草酸可逆转哮喘模型小鼠上述病理变化,且高剂量积雪草酸作用更强。Colivelin 可减弱积雪草酸对哮
喘模型小鼠上述病理变化的作用。结论:积雪草酸可通过减弱IL-6 表达与STAT3、NF-κB 的磷酸化,抑制哮喘小鼠炎症细胞及
炎症因子产生,从而减轻气道炎症及肺组织损伤,改善肺功能。 |
| 关键词: 积雪草酸 白细胞介素-6/ 信号转导子和转录激活子3/ 核转录因子-κB 哮喘 Treg/ Th17 免疫平衡 |
| DOI：doi:10.13407/j.cnki.jpp.1672-108X.2024.10.002 |
|
| 基金项目::广西壮族自治区中医药管理局自筹经费科研课题,编号20210036;2022 年广西国际壮医医院“青苗工程”培育项目“青年拔尖人
才”项目。 |
|
| Effects of Asiatic Acid on Treg / Th17 Immune Balance in Asthmatic Mice by Regulating Interleukin-6/Signal Transductor and Transcription Activator 3 / Nuclear Transcription Factor-κB Pathway |
| Peng Xian1, Zou Min2, Yang Yubin1 |
| ((1. Jingzhou Hospital of Traditional Chinese Medicine, Hubei Jingzhou 434000, China; 2.
Guangxi International Zhuang Medicine Hospital, Guangxi International Zhuang Medicine Hospital Affiliated to Guangxi University of
Chinese Medicine, Nanning 530201, China)) |
| Abstract: |
| Objective: To probe into the effects of asiatic acid on Treg/ Th17 immune balance in asthmatic mice by regulating
interleukin-6 (IL-6) / signal transducer and activator of transcription-3 (STAT3) / nuclear transcription factor-κB (NF-κB) pathway.
Methods: Asthmatic mice models were prepared by sensitization and stimulation with ovalbumin (OVA), and randomly divided into the
model group, low-dose (54 mg/ kg) asiatic acid group, high-dose (108 mg/ kg) asiatic acid group, high-dose (108 mg/ kg) asiatic acid+
Colivelin (IL-6/ STAT3/ NF-κB activator, 2 mg/ kg) group, with 10 mice in each group, another 10 mice were selected and given equal
doses of physiological saline during the sensitization and stimulation stages as the control group. Pathological morphology of pulmonary
tissue, number of inflammatory cells in bronchoalveolar lavage fluid (BALF), levels of Treg/ Th17 in peripheral blood, levels of Treg,
Th17 cell secretion factors in BALF and serum, and expression of IL-6/ STAT3/ NF-κB pathway related proteins in pulmonary tissue were
detected after treating with asiatic acid and Colivelin. Results: Compared with the control group, the pulmonary tissue of mice in the
model group showed great pathological damage, the proportion of Treg cells and Treg/ Th17 in peripheral blood, levels of IL-10 and IL-35
in BALF and serum levels decreased (P<0. 05), the pulmonary inflammation score, white blood cell count and eosinophil count in BALF,
proportion of Th17 cells in peripheral blood, levels of IL-17 and IL-6 in BALF and serum, IL-6 protein expression and p-STAT3/ STAT3,
p-NF-κB p65/ NF-κB p65 in pulmonary tissue increased (P<0. 05). Low-dose and high-dose asiatic acid reversed the above pathological
changes in asthmatic mice models, and the effect of asiatic acid was stronger at higher doses. Colivelin could attenuate the pathological
changes mentioned above in asthma model mice induced by asiatic acid. Conclusion: Asiatic acid can inhibit the production of
inflammatory cells and inflammatory factors by decreasing the expression of IL-6 and the phosporylation of STAT3 and NF-κB in asthmatic
mice, thereby reducing airway inflammation and pulmonary tissue damage and improving pulmonary function. |
| Key words: asiatic acid interleukin-6/ signal transductor and transcription activator 3/ nuclear transcription factor-κB asthma Treg/ Th17 immune balance |
